Control-theoretic immune tradeoffs explain SARS-CoV-2 virulence and transmission variation
Abstract
Dramatic variation in SARS-CoV-2 virulence and transmission between hosts has driven the COVID-19 pandemic. The complexity and dynamics of the immune response present a challenge to understanding variation in SARS-CoV-2 infections. To address this challenge, we apply control theory, a framework used to study complex feedback systems, to establish rigorous mathematical bounds on immune responses. Two mechanisms of SARS-CoV-2 biology are sufficient to create extreme variation between hosts: (1) a sparsely expressed host receptor and (2) potent, but not unique, suppression of interferon. The resulting model unifies disparate and unexplained features of the SARS-CoV-2 pandemic, predicts features of future viruses that threaten to cause pandemics, and identifies potential interventions.
Additional Information
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license. This version posted April 26, 2021.Attached Files
Submitted - 2021.04.25.441372v1.full.pdf
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Additional details
- Eprint ID
- 108865
- Resolver ID
- CaltechAUTHORS:20210429-095332336
- Created
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2021-04-29Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field
- Caltech groups
- COVID-19